A case report of undetected cardiac arrest in a patient with an insertable cardiac monitor.

Insertable cardiac monitors (ICMs) are small electrocardiographs implanted subcutaneously to automatically record electrocardiograms when arrhythmia is detected in patients with syncope. If the ICM misses a significant arrhythmia, it may delay the diagnosis of arrhythmogenic syncope and put the patient at risk. Herein, we describe a case of undetected cardiac arrest in a patient with ICM. An 87-year-old man with syncope was admitted to the hospital. After 8 days of monitoring, the cause could not be determined, and an ICM was implanted. Nine hours after implantation, the patient experienced cardiopulmonary arrest. Despite a body surface electrocardiogram showing ventricular flatline and fibrillation, the ICM failed to record. The cause of failure to record was considered to be the fluctuation in the R-wave amplitude of the ICM and noise oversensing. In conclusion, albeit infrequently, ICMs might overlook life-threatening arrhythmias. Even in cases where the ICM fails to detect an arrhythmia matching the symptoms, it may not be feasible to entirely rule out the presence of arrhythmias. Learning objective: Insertable cardiac monitors (ICMs) are used to diagnose arrhythmogenic syncope. However, extremely infrequently, ICM may fail to record life-threatening arrhythmias. Failure to capture arrhythmias can happen due to an unfortunate combination of factors such as a low amplitude of the recorded R wave and noise. Even in cases where the ICM does not detect an arrhythmia that matches the symptoms, it may not be feasible to completely exclude the presence of arrhythmias.

[Control of Posture and Gait by the Basal Ganglia: Pathophysiological Mechanisms Implicated in Parkinson's Disease].

Regulation of posture-gait control by the basal ganglia (BG) plays a critical role in the acquisition of automatically executed context-dependent learned motor acts, technically referred to as habit formation. Patients with Parkinson's disease (PD) show posture-gait disturbances and progressively lose habitual behaviors. Injury to dopamine (DA) neurons in the midbrain is implicated as the primary pathophysiological mechanism underlying PD; therefore, DA actions in the BG play a pivotal role in optimal BG function. In this commentary, we discuss the mechanism underlying BG-modulated regulation of cognitive posture-gait control by the cerebral cortex through the cortico-BG loop and the basic posture-gait mechanisms underlying the actions of the brainstem and spinal cord via the BG-brainstem projection. The BG primarily regulates excitability of the cerebral cortex and brainstem through its DA-mediated inhibitory action. Based on these considerations, we describe the pathophysiological mechanisms that contribute to posture-gait disturbances in PD. Recent clinical studies suggest that posture-gait disturbances may be attributable to functional disconnection between the BG and the cerebral cortex and brainstem. Injury to various neurotransmitter systems in addition to the DA system and significant alpha-synuclein (Lewy body)-induced degeneration of the brainstem neurons may worsen posture-gait control impairment in PD.

Knee dynamics during take-off and landing in spike jumps performed by volleyball players with patellar tendinopathy.

[Purpose] Patellar tendinopathy is a common sports injury. The risk factors for this injury can be categorized as intrinsic, extrinsic, and dynamic. We examined the dynamic factors in this study. [Participants and Methods] The participants were volleyball players who were assigned to a patient group (n=6) if they had medial patellar tendinopathy in the left knee or to a control group (n=7) otherwise. The participants performed spike jumps, and their ground reaction force and three-dimensional kinematic data were recorded. Knee angle and moment data were extracted at the peak extension moment of take-off and landing. [Results] The two groups showed no differences in knee angles. A tendency for abduction/external rotation moments at take-off and landing on both sides was observed in the control group, while the patient group showed adduction and internal rotation moments at take-off and adduction moment at landing in the left (injured) knee. [Conclusion] The observed knee joint moments in the left (injured) knee of the patient group may have been involved in the pathophysiological mechanism underlying the development of patellar tendinopathy.

Preceding Postural Control in Forelimb Reaching Movements in Cats.

Postural control precedes the goal-directed movement to maintain body equilibrium during the action. Because the environment continuously changes due to one's activity, postural control requires a higher-order brain function that predicts the interaction between the body and the environment. Here, we tried to elucidate to what extent such a preceding postural control (PPC) predictively offered a posture that ensured the entire process of the goal-directed movement before starting the action. For this purpose, we employed three cats, which we trained to maintain a four-leg standing posture on force transducers to reach the target by either forelimb. Each cat performed the task under nine target locations in front with different directions and distances. As an index of posture, we employed the center of pressure (CVP) and examined CVP positions when the cat started postural alteration, began to lift its paw, and reached the target. After gazing at the target, each cat started PPC where postural alteration was accompanied by a 20-35 mm CVP shift to the opposite side of the forelimb to be lifted. Then, the cat lifted its paw at the predicted CVP position and reached the forelimb to the target with a CVP shift of only several mm. Moreover, each cat had an optimal target location where the relationship between the cat and target minimized the difference in the CVP positions between the predicted and the final. In this condition, more than 80% of the predicted CVP positions matched the final CVP positions, and the time requiring the reaching movement was the shortest. By contrast, the forelimb reaching movement required a greater CVP shift and longer time when the target was far from the cat. In addition, the time during forelimb reaching showed a negative correlation with the speed of the CVP shift during the PPC. These results suggest that the visuospatial information, such as the body-environment interaction, contributes to the motor programming of the PPC. We conclude that the PPC ensures postural stability throughout the action to optimize the subsequent goal-directed movements. Impairments in these processes may disturb postural stability during movements, resulting in falling.

Protease-activated receptor-stimulated interleukin-6 expression in endometriosis-like lesions in an experimental mouse model of endometriosis.

The present study was undertaken to investigate the function of protease-activated receptor (PAR) in endometriotic lesions using a mouse model of endometriosis. Unilateral ovariectomy (uOVX) was performed on female nude mice followed by intraperitoneal transplantation of a suspension mixture of immortalized human endometrial epithelial cells (EM-1) and stromal cells (EtsT-499). Endometriosis-like lesions were observed mostly around the dissection site after transplantation. The expression of interleukin (IL)-6 and cyclooxygenase-2 in the lesions was enhanced in uOVX mice compared to non-uOVX animals. In non-uOVX mice, IL-6 mRNA levels were higher in lesions formed with cells that were pretreated with PAR1/2 agonists (thrombin, 10 U/ml and PAR2-activating peptide, 30 µM) compared to untreated, intact cells. Peritoneal IL-6 concentrations were also increased in the PAR1/2 agonists-treated group. IL-6 expression induced by PAR activation was blocked by the treatment of cells with serine protease inhibitors. In cultured endometrial cells, simultaneous treatment with PAR1 and PAR2 agonists significantly increased the expression of IL-6. These results suggest that peritoneal bleeding may accelerate IL-6 expression in endometriotic lesions in part through the activation of PAR.